Exercise training improves the net balance of cardiac Ca'EXP2+' handling protein expression in heart failure (2007)
- Autores:
- Autores USP: KRIEGER, EDUARDO MOACYR - FM ; KRIEGER, JOSE EDUARDO - FM ; NEGRÃO, CARLOS EDUARDO - EEFE ; BRUM, PATRICIA CHAKUR - EEFE
- Unidades: FM; EEFE
- DOI: 10.1152/physiolgenomics.00188.2006
- Assunto: FISIOLOGIA DO EXERCÍCIO
- Idioma: Inglês
- Resumo: ET in ('alfa''2 IND.A' /'alfa''2 IND.C'ARKO) mice improved exercise tolerance and systolic function. ET slightly reduced cardiac myocyte width, but unchanged ventricular fibrosis in ('alfa''2 IND.A' /'alfa''2 IND.C'ARKO) mice. ET significantly increased the expression of SERCA2 (20%) and phospho-Ser'EXP16`-PLN (63%), phospho-Thr'EXP17'-PLN (211%) in congenic ('alfa''2 IND.A' /'alfa''2 IND.C'ARKO) mice. Furthermore, ET restored NCX and PP1 expression in ('alfa''2 IND.A' /'alfa''2 IND.C'ARKO) to untrained WT mice levels. Thus, we provide evidence that Ca'EXP2+' handling is impaired in this HF model and that overall VF improved upon ET, which was associated to changes in the net balance of cardiac Ca'EXP2+' handling proteinsThe molecular basis of the beneficial effects associated with exercise training (ET) on overall ventricular function (VF) in heart failure (HF) remains unclear. We investigated potential Ca'EXP2+' handling abnormalities and whether ET would improve VF of mice lacking 'alfa''2 IND.A' and 'alfa''2 IND.C'-adrenoceptors ('alfa''2 IND.A' /'alfa''2 IND.C'ARKO) that have sympathetic hyperactivity-induced HF. A cohort of male wild-type (WT) and congenic ('alfa''2 IND.A' /'alfa''2 IND.C'ARKO) mice in a C57BL/J genetic background (5-7 mo of age) was randomly assigned into untrained and trained groups. VF was assessed by two-dimensional guided M-mode echocardiography. Cardiac myocyte width and ventricular fibrosis were evaluated with a computer-assisted morphometric system. Sarcoplasmic reticulum Ca'EXP2+' ATPase (SERCA2), phospholamban (PLN), phospho-Ser'EXP16`-PLN, phospho-Thr'EXP17'-PLN, phosphatase 1 (PP1), and Na+-Ca'EXP2+' exchanger (NCX) were analyzed by Western blotting. ET consisted of 8-wk running sessions of 60 min, 5 days/wk. ('alfa''2 IND.A' /'alfa''2 IND.C'ARKO) mice displayed exercise intolerance, systolic dysfunction, increased cardiac myocyte width, and ventricular fibrosis paralleled by decreased SERCA2 and increased NCX expression levels
- Imprenta:
- Fonte:
- Título do periódico: Physiological genomics
- Volume/Número/Paginação/Ano: v. 29, n. 3, p. 246-252, mai. 2007
- Este periódico é de assinatura
- Este artigo NÃO é de acesso aberto
- Cor do Acesso Aberto: closed
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ABNT
ROLIM, Natale Pinheiro Lage et al. Exercise training improves the net balance of cardiac Ca'EXP2+' handling protein expression in heart failure. Physiological genomics, v. 29, n. 3, p. 246-252, 2007Tradução . . Disponível em: https://doi.org/10.1152/physiolgenomics.00188.2006. Acesso em: 18 set. 2024. -
APA
Rolim, N. P. L., Medeiros, A., Rosa, K. T., Mattos, K. C., Irigoyen, M. C., Krieger, E. M., et al. (2007). Exercise training improves the net balance of cardiac Ca'EXP2+' handling protein expression in heart failure. Physiological genomics, 29( 3), 246-252. doi:10.1152/physiolgenomics.00188.2006 -
NLM
Rolim NPL, Medeiros A, Rosa KT, Mattos KC, Irigoyen MC, Krieger EM, Krieger JE, Negrão CE, Brum PC. Exercise training improves the net balance of cardiac Ca'EXP2+' handling protein expression in heart failure [Internet]. Physiological genomics. 2007 ; 29( 3): 246-252.[citado 2024 set. 18 ] Available from: https://doi.org/10.1152/physiolgenomics.00188.2006 -
Vancouver
Rolim NPL, Medeiros A, Rosa KT, Mattos KC, Irigoyen MC, Krieger EM, Krieger JE, Negrão CE, Brum PC. Exercise training improves the net balance of cardiac Ca'EXP2+' handling protein expression in heart failure [Internet]. Physiological genomics. 2007 ; 29( 3): 246-252.[citado 2024 set. 18 ] Available from: https://doi.org/10.1152/physiolgenomics.00188.2006 - O treinamento físico previne a disfunção cardíaca e altera a recaptação de cálcio em um modelo genético de cardiomiopatia induzida por hiperatividade simpática
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Informações sobre o DOI: 10.1152/physiolgenomics.00188.2006 (Fonte: oaDOI API)
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